In the white population, an inherited gene-defective disease known as cystic fibrosis is encountered with a frequency of 1/1000-2000. This disease is caused by the defect of a gene coding for cystic fibrosis transmembrane conductance regulator (CFTR) protein and in the event of bacterial infection to the respiratory organ with mucoid forms of Pseudomonas aeruginosa,. Mucous substances collect in the lungs to cause an obstruction of airways leading to premature death. Though antibiotics and digestive enzymes are currently in use for the treatment of this disease, adequate therapeutic responses remain to be achieved as yet.
Recently (Richard C. Hubbard, et al.) have reported that symptomatic improvements in cystic fibrosis may be expected if the DNA contained in said mucus is lysed with a DNase [The New England Journal of Medicine 326, 812-815, 1992]. However, the DNase is little capable of lysing the mucus produced by bacteria of the genus Pseudomonas so that no sufficient efficacy can be expected.
Meanwhile, it is not deniable that the action of antibiotics and digestive enzymes on Pseudomonas aeruginosa is compromised by the alginate which these microorganisms themselves produce.